Imatinib induces durable hematologic and cytogenetic responses in patients with accelerated phase chronic myeloid leukemia: results of a phase 2 study.
By M. Talpaz, R. Silver, Brian J. Druker, J. Goldman, C. Gambacorti-Passerini, F. Guilhot, C. Schiffer, T. Fischer, M. Deininger, A. Lennard and 12 more. Blood, 2002
1,073 citations recorded by the source corpus.
Subfields: Genetics, Hematology, Public Health, Environmental and Occupational Health
View Paper: https://www.semanticscholar.org/paper/8b19a8ad9c5597c28d87eec8d6b282303b501605
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Citations in the corpus
- Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia. (2007, background): “Durable responses are the rule in early chronic phase, but the exception in blast crisis.(1,6,7) Responses to second-line inhibitors (dasatinib(11,38,39,50) and nilotinib(10,41)) are based on limited preliminary evidence (green trace).”
- Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia. (2002, background): “…treatment after striking efficacy was demonstrated in all stages of the disease (Druker et al., sion in CML. Detailed analysis of 11 such patients revealed at least two distinct mechanisms for resistance—BCR-ABL gene2001a, 2001b; Kantarjian et al., 2002; Sawyers et al., 2002; Talpaz et al., 2002).”
- Detection of BCR-ABL mutations in patients with CML treated with imatinib is virtually always accompanied by clinical resistance, and mutations in the ATP phosphate-binding loop (P-loop) are associated with a poor prognosis. (2003, background): “increased (3), MBC (11); died in MBC (15); the”
- BCR-ABL tyrosine kinase inhibitors in the treatment of Philadelphia chromosome positive chronic myeloid leukemia: a review. (2010, methodology): “[62] Talpaz M, Silver RT, Druker BJ, Goldman JM, Gambacorti-Passerini C, Guilhot F, et al.”